کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5526886 1401554 2017 12 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Benzyl alcohol induces a reversible fragmentation of the Golgi apparatus and inhibits membrane trafficking between endosomes and the trans-Golgi network
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی تحقیقات سرطان
پیش نمایش صفحه اول مقاله
Benzyl alcohol induces a reversible fragmentation of the Golgi apparatus and inhibits membrane trafficking between endosomes and the trans-Golgi network
چکیده انگلیسی


- Benzyl alcohol inhibits retrograde traffic from endosomes to the trans-Golgi network.
- Benzyl alcohol induces fragmentation of the Golgi apparatus.
- Reduced toxicity of Shiga toxin, and ricin in benzyl alcohol treated cells.
- The toxic effect of diphtheria toxin is decreased in benzyl alcohol treated cells.
- The number of acidic compartments is reduced by benzyl alcohol.

Benzyl alcohol (BnOH) is widely used as a component of foods, cosmetics, household products and medical products. It is generally considered to be safe for human use, however, it has been connected to a number of adverse effects, including hypersensitivity reactions and neonatal deaths. BnOH is a membrane fluidizing agent that can affect membrane protein activity and cellular processes such as ligand binding to cell surface receptors, endocytosis and degradation of lysosomal cargo. In this study, we examined the effects of BnOH on intracellular transport using Shiga toxin (Stx), diphtheria toxin (DT) and ricin. BnOH caused reduced toxicity of all three toxins at BnOH concentrations that cause membrane fluidization. The reduced toxicity of Stx and ricin was mainly due to inhibition of retrograde transport between endosomes and the trans-Golgi network as BnOH had small effects on cell association and endocytosis of ricin and Stx. Strikingly, BnOH also induced a reversible fragmentation of the Golgi apparatus.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Cell Research - Volume 357, Issue 1, 1 August 2017, Pages 67-78
نویسندگان
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